In conclusion this study detected

In conclusion, this study detected the expression of adiponectin and its receptors, AdipoR1 and AdipoR2, in goat ovarian follicles. In addition, adiponectin was shown to enhance the progression of goat oocyte nuclear maturation in vitro. The present findings provide evidence for paracrine/autocrine effects of the analyzed hormone. However, future studies are needed to elucidate the mechanisms underlying the effect of adiponectin on meiotic maturation and to understand the role of the adiponectin system in goat fertility.
Declaration of interest
Acknowledgements The authors thank FACEPE (Fundação de Amparo à Ciência e Tecnologia do Estado de Pernambuco)FACEPE for financial support (APQ-1115-5.05/14).
Introduction Adipokines, a group of proteins synthesized in adipose tissue, have attracted a considerable interest due to their potential role in the development of cancer as a risk factor. Two adipokines, leptin, and adiponectin in particular, have come to be recognized for their influence on tumor biology. Physiological and pathological relationships of leptin and adiponectin are largely contradictory to each other, in terms of their effects on proliferative activities of malignant tachykinins [1], [2], [3]. Leptin appears to play an important role in immunity and hematopoiesis. It exerts proliferative and antiapoptotic activities in variety of cell types, including T lymphocytes, leukemia cells, and hematopoietic progenitors [4], [5]. These biological actions of leptin are carried out through interaction with its specific surface receptor OB-R, resulting in the activation of divergent signal transduction pathways, such as the mitogen-activated-protein kinase (MAPK), nuclear factor-kB (NF-kB), and signal transducers and activators of transcription (STAT), which eventually induce expression of several genes involved in proliferation and differentiation [6], [7], [8], [9]. Several alternatively spliced isoforms of leptin receptor (OB-R) have been reported: two main leptin receptor isoforms dominate, the long (OB-Rb) and short subtypes (OB-Ra) sharing extracellular and transmembrane domains, but differing in intracellular C-terminal tails [10]. The expression of OB-R has been reported in platelets, CD4+ and CD8+ T lymphocytes, CD34+ hematopoietic stem cells and peripheral blood mononuclear cells [4], [11], [12]. Earlier studies have shown expression of leptin receptor in leukemia cells from patients with acute myeloblastic leukemia (AML), acute lymphoblastic leukemia (ALL), and chronic myeloid leukemia (CML), and also their higher expression in blast crisis than chronic phase in CML were reported [12], [13]. On the other hand, adiponectin has been found to be an important negative regulator of hematopoiesis and immune system. There is convincing evidence that adiponectin also has modulated cell proliferation and apoptosis [2], [14]. It was found that adiponectin predominantly inhibits proliferation of myeloid cell lines, and induces apoptosis in myelomonocytic leukemia lines, but did not suppress proliferation of erythroid or lymphoid cell lines. Its effects seem to be mediated by two distinct receptors: the adiponectin receptor-1 (AdipoR1), ubiquitously expressed with highest abundance in skeletal muscle, and adiponectin receptor-2 (AdipoR2), most abundantly expressed in liver. These receptors are known to activate adenosine 5′-monophosphate-activated protein kinase (AMPK), MAPK, and NF-kB signaling pathways [1], [15]. We and others have recently demonstrated that circulating adiponectin was inversely associated with risk for AML [16], [17], but not with ALL in children [17]. In addition, it was reported that adiponectin treatment suppresses the growth of myelomonocytic cells [14]. Leptin receptors were shown to play a proliferative role in normal myeloid development [12], [13], whereas it was reported that adiponectin suppresses the growth of human myelomonocytic cells, inducing apoptosis in myelomonocyctic progenitor cells (leukemia lines) in vitro[14]. These data clearly suggest the relevance of leptin/OB-R and adiponectin/AdipoR signaling to tumorigenesis, in particular to leukemias.